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EGFR — SOCS1

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: SOCS1 — EGFR (physical association, affinity chromatography technology) Xia et al., J Biol Chem 2002*
• IRef Hprd Interaction: SOCS1 — EGFR (in vivo) Xia et al., J Biol Chem 2002*
• IRef Ophid Interaction: SOCS1 — EGFR (aggregation, interologs mapping) Brown et al., Bioinformatics 2005
• IRef Ophid Interaction: SOCS1 — EGFR (aggregation, confirmational text mining) Xia et al., J Biol Chem 2002*

Text-mined interactions from Literome

Flowers et al., J Immunol 2004 : Tkip also inhibited epidermal growth factor receptor autophosphorylation, consistent with the fact that epidermal growth factor receptor is regulated by SOCS-1 and SOCS-3, similar to JAK2
Lee et al., Mol Cancer Ther 2006 (Carcinoma, Squamous Cell...) : Epigenetic modification of SOCS-1 differentially regulates STAT3 activation in response to interleukin-6 receptor and epidermal growth factor receptor signaling through JAK and/or MEK in head and neck squamous cell carcinomas ... Suppressor of cytokine signaling-1 ( SOCS-1 ) has been implicated recently in the negative regulation of IL-6R/Janus activated kinase ( JAK ) -mediated activation of STAT3, suggesting that SOCS-1 could affect alternative activation of STAT3 by EGFR , IL-6R, and associated kinases ... We investigated whether epigenetic modification of SOCS-1 affects STAT3 activation in response to IL-6R-, EGFR- , JAK-, or mitogen activated protein kinase/extracellular signal regulated kinase kinase ( MEK ) -mediated signal activation
Wang et al., Breast Cancer Res 2008 (Breast Neoplasms) : Since epidermal growth factor receptor (EGFR), like S100A7, is often expressed in estrogen receptor-alpha negative ( ERalpha- ) breast cancer, we set out to investigate the role of Jab1 in mediating EGFR signaling, another facet of the ERalpha- phenotype